PubMed · 7488501
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G C Fenn, S Ratcliffe. 1995. Tramadol.. https://doi.org/10.1093/bja%2F75.4.501
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The application of thermal noxious stimuli forms the basis of some widely used tests to detect either hyperalgesic or analgesic reactions. In the classical hot plate test, mice react by licking their paws and/or jumping. However, tests relying on the unilateral application of thermal radiant heat to the plantar side of the hindpaw, have become popular in recent years since unilateral changes in nociceptive sensitivity can be detected. Based on the aforementioned tests, we developed a testing procedure in mice, the unilateral hot plate (UHP): the plantar side of one hindpaw is placed on a hot plate surface and, thus, the withdrawal latency of each paw can be measured separately. The effectiveness of several analgesic and hyperalgesic drugs measured by the UHP was compared with that measured by a method based on the application of radiant heat (RH) stimuli. In the UHP method, morphine (1-10 mg/kg) increases latencies, while spinal NMDA (0.001-1 ng) or PGE2 (30-300 ng), intraplantar carrageenan (2 - 4%) or PGE2 (30-300 ng) decrease latencies. In all cases, the UHP method detected changes in pain reactivity at lower doses than the RH test. The sensitivity and usefulness of the UHP test for performing pain studies in mice is described.
The treatment of pain before it initiates may prevent the persistent pain-induced changes in the central nervous system that amplify pain long after the initial stimulus. The effects of pre- or postoperative intraperitoneal administration of morphine (2 to 8 mg/kg), dipyrone (40 and 80 mg/kg), diclofenac (2 to 8 mg/kg), ketoprofen (10 and 20 mg/kg), and tenoxicam (10 and 20 mg/kg) were studied in a rat model of post-incisional pain. Groups of 5 to 8 male Wistar rats (140-160 g) were used to test each drug dose. An incision was made on the plantar surface of a hind paw and the changes in the withdrawal threshold to mechanical stimulation were evaluated with Von Frey filaments at 1, 2, 6 and 24 h after the surgery. Tenoxicam was given 12 or 6 h preoperatively, whereas the remaining drugs were given 2 h or 30 min preoperatively. Postoperative drugs were all given 5 min after surgery. No drug abolished allodynia when injected before or after surgery, but thresholds were significantly higher than in control during up to 2 h following ketoprofen, 6 h following diclofenac, and 24 h following morphine, dipyrone or tenoxicam when drugs were injected postoperatively. Significant differences between pre- and postoperative treatments were obtained only with ketoprofen administered 30 min before surgery. Preoperative (2 h) intraplantar, but not intrathecal, ketoprofen reduced the post-incisional pain for up to 24 h after surgery. It is concluded that stimuli generated in the inflamed tissue, rather than changes in the central nervous system are relevant for the persistence of pain in the model of post-incisional pain.
Administration of mu-opioid receptor subtype agonists into the nucleus accumbens shell elicits feeding which is dependent upon the normal function of mu-, delta- and kappa-opioid receptors, D(1) dopamine receptors and GABA(B) receptors in the nucleus accumbens shell for its full expression. Whereas the AMPA antagonist, DNQX administered into the nucleus accumbens shell elicits a transient, though intense feeding response, feeding is elicited by excitatory amino acid agonists administered into the lateral hypothalamus. The present study examined whether excitatory amino acid agonists elicited feeding following administration into the nucleus accumbens shell of rats, whether such feeding responses were altered by opioid antagonist pretreatment, and whether such feeding responses interacted with feeding elicited by mu-opioid agonists. Both AMPA (0.25-0.5 microg) and NMDA (1 microg) in the nucleus accumbens shell significantly and dose-dependently increased food intake over 4 h. Both feeding responses were blocked by naltrexone pretreatment in the nucleus accumbens shell. The mu-opioid agonist, [D-Ala(2),NMe-Phe(4),Gly-ol(5)]-enkephalin in the nucleus accumbens shell significantly increased food intake which was significantly enhanced by AMPA cotreatment. This enhanced feeding response was in turn blocked by pretreatment with either general or mu-selective opioid antagonists. In contrast, cotreatment of NMDA and the mu-opioid agonist in the nucleus accumbens shell elicited feeding which was significantly less than that elicited by either treatment alone. These data indicate the presence of important interactions between excitatory amino acid receptors and mu-opioid receptors in the nucleus accumbens shell in mediating feeding responses in nondeprived, ad libitum-fed rats.